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The expression of cardiac protein tyrosine phosphatases 1B (PTP1B) was decreased in the type 2 diabetic mice with Astragalus polysaccharide therapy
Author(s) -
Mao Xianqing,
Yang Jingping Ou,
Wang Nian,
Zou Feng,
Wang Sheng,
Zhang Cheng
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a793-b
Subject(s) - medicine , endocrinology , insulin , streptozotocin , diabetic cardiomyopathy , insulin resistance , diabetes mellitus , protein tyrosine phosphatase , insulin receptor , heart failure , cardiomyopathy , receptor
Our previous study showed that Astragalus polysaccharide (APS) had a good insulin‐sensitizing and hypoglycemic activity by decreasing the elevated expression and activity of PTP1B in the skeletal muscles of T2DM rats. But its potential effect on the expression of cardiac protein tyrosine phosphatase 1B (PTP1B) is still unknown. Thus the high fat‐fed streptozotocin (STZ,25mg/kg, ip)‐treated rats, an animal model of type 2 diabetes mellitus (T2DM) were established and treated with APS (400 mg/kg p.o.) for 5 weeks. Insulin sensitivity was identified by Oral Glucose Tolerance Test (OGTT) and HOMA‐IR index. Further analysis included blood sugar, glycosylated hemoglobin and serum insulin was performed by commercial kits. Pathological variation of heart was observed by microscope with HE staining. Cardiac PTP1B expression was detected by Immunoprecipitation or Western blotting. In this study, the diabetic rats responded to APS with a significant decrease in plasma glucose, glycosylated hemoglobin and improved insulin sensitivity. In the T2DM rats, myocardial cell hypertrophy and interstitial edema was found. Notably, the expression of PTP1B was increased and the insulin signaling in cardiac muscle was disturbed in diabetic rats. The results showed that APS treatment reduced the pathological variation and PTP1B protein level of the heart. Therefore, APS can ameliate cardiac insulin signal transduction, which was probably realized by expression inhibition of PTP1B in T2DM rats. This research is supported by National Nature Science Fund of China (30370673).